Three monkeys performed a visually guided reach-touch task with and without laterally displacing prisms. The prisms offset the normally aligned gaze/reach and subsequent touch. Naive monkeys showed adaptation, such that on repeated prism trials the gaze-reach angle widened and touches hit nearer the target. On the first subsequent no-prism trial the monkeys exhibited an aftereffect, such that the widened gaze-reach angle persisted and touches missed the target in the direction opposite that of initial prism-induced error. After 20-30 days of training, monkeys showed long-term learning and storage of the prism gaze-reach calibration: they switched between prism and no-prism and touched the target on the first trials without adaptation or aftereffect. Injections of lidocaine into posterolateral cerebellar cortex or muscimol or lidocaine into dentate nucleus temporarily inactivated these structures. Immediately after injections into cortex or dentate, reaches were displaced in the direction of prism-displaced gaze, but no-prism reaches were relatively unimpaired. There was little or no adaptation on the day of injection. On days after injection, there was no adaptation and both prism and no-prism reaches were horizontally, and often vertically, displaced. A single permanent lesion (kainic acid) in the lateral dentate nucleus of one monkey immediately impaired only the learned prism gaze-reach calibration and in subsequent days disrupted both learning and performance. This effect persisted for the 18 days of observation, with little or no adaptation.

Complex (CS)- and simple-spike (SS) discharge from single Purkinje cells (Pc) in the posterolateral cerebellum of two monkeys was recorded during a visually guided reach-touch task. A visual target appeared (TA) off-gaze at a random location on a screen. On initiation of arm reach, the target disappeared, then reappeared (TR) after a fixed delay. TR was either at the same location (baseline condition) or a shifted location at a fixed distance and direction from TA location (shift condition). Across trials, we observed one or two peaks of CS activity, depending on the reach condition. The first CS (T1 CS) peak was tuned to the location of TA on the screen, following TA by approximately 150 ms. The second CS (T2 CS) peak occurred only in the shift condition, was tuned to the shift location of TR, and followed TR by approximately 150 ms. The locational preferences of T1 and T2 CS peaks were the same. T1 and T2 CSs preceded saccades to TA and TR at the preferred location and occurred during reaches with either arm. T1 CSs occurred during trials in which the target appeared, and there was a saccade to target, but no subsequent arm reach followed. SS firing varied with TA/TR in the same preferred location as for the accompanying CS. We conclude that posterolateral Pc CS and SS firing changes following an off-gaze visual target appearance in a preferred location when there is a subsequent saccade to that location.

Therapeutic study, level III.

BackgroundTactical Combat Casualty Care guidelines for hemorrhage recommend resuscitation to systolic blood pressure (SBP) of 85±5 mm Hg during prehospital care. Success depends on transport to definitive care within the ‘golden hour’. As future conflicts may demand longer prehospital/transport times, we sought to determine safety of prolonged permissive hypotension (PH).MethodsAdult male swine were randomized into three experimental groups. Non-shock (NS)/normotensive underwent anesthesia only. NS/PH was bled to SBP of 85±5 mm Hg for 6 hours of prolonged field care (PFC) with SBP maintained via crystalloid, then recovered. Experimental group underwent controlled hemorrhage to mean arterial pressure 30 mm Hg until decompensation (Decomp/PH), followed by 6 hours of PFC. Hemorrhaged animals were then resuscitated with whole blood and observed for 24 hours. Physiologic variables, blood, tissue samples, and neurologic scores were collected.ResultsSurvival of all groups was 100%. Fluid volumes to maintain targeted SBP in PFC were significantly higher in the hemorrhage group than sham groups. After 24 hours’ recovery, no significant differences were observed in neurologic scores or cerebrospinal fluid markers of brain injury. No significant changes in organ function related to treatment were observed during PFC through recovery, as assessed by serum chemistry and histological analysis.ConclusionsAfter 6 hours, a prolonged PH strategy showed no detrimental effect on survival or neurologic outcome despite the increased ischemic burden of hemorrhage. Significant fluid volume was required to maintain SBP—a potential logistic burden for prehospital care. Further work to define maximum allowable time of PH is needed.Study typeTranslational animal model.Level of evidenceN/A.